Lack of miRNA Misregulation at Early Pathological Stages in Drosophila Neurodegenerative Disease Models.
Identifieur interne : 000795 ( PubMed/Checkpoint ); précédent : 000794; suivant : 000796Lack of miRNA Misregulation at Early Pathological Stages in Drosophila Neurodegenerative Disease Models.
Auteurs : Anita Reinhardt [France] ; Sébastien Feuillette ; Marlène Cassar ; Céline Callens ; Hélène Thomassin ; Serge Birman ; Magalie Lecourtois ; Christophe Antoniewski ; Hervé TricoireSource :
- Frontiers in genetics [ 1664-8021 ] ; 2012.
Abstract
Late onset neurodegenerative diseases represent a major public health concern as the population in many countries ages. Both frequent diseases such as Alzheimer disease (AD, 14% incidence for 80-84 year-old Europeans) or Parkinson disease (PD, 1.4% prevalence for >55 years old) share, with other low-incidence neurodegenerative pathologies such as spinocerebellar ataxias (SCAs, 0.01% prevalence) and frontotemporal lobar degeneration (FTLD, 0.02% prevalence), a lack of efficient treatment in spite of important research efforts. Besides significant progress, studies with animal models have revealed unexpected complexities in the degenerative process, emphasizing a need to better understand the underlying pathological mechanisms. Recently, microRNAs (miRNAs), a class of small regulatory non-coding RNAs, have been implicated in some neurodegenerative diseases. The current data supporting a role of miRNAs in PD, tauopathies, dominant ataxias, and FTLD will first be discussed to emphasize the different levels of the pathological processes which may be affected by miRNAs. To investigate a potential involvement of miRNA dysregulation in the early stages of these neurodegenerative diseases we have used Drosophila models for seven diseases (PD, 3 FTLD, 3 dominant ataxias) that recapitulate many features of the human diseases. We performed deep sequencing of head small RNAs after 3 days of pathological protein expression in the fly head neurons. We found no evidence for a statistically significant difference in miRNA expression in this early stage of the pathological process. In addition, we could not identify small non-coding CAG repeat RNAs (sCAG) in polyQ disease models. Thus our data suggest that transcriptional deregulation of miRNAs or sCAG is unlikely to play a significant role in the initial stages of neurodegenerative diseases.
DOI: 10.3389/fgene.2012.00226
PubMed: 23115562
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first="Christophe" last="Antoniewski">Christophe Antoniewski</name></author><author><name sortKey="Tricoire, Herve" sort="Tricoire, Herve" uniqKey="Tricoire H" first="Hervé" last="Tricoire">Hervé Tricoire</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="RBID">pubmed:23115562</idno><idno type="pmid">23115562</idno><idno type="doi">10.3389/fgene.2012.00226</idno><idno type="wicri:Area/PubMed/Corpus">000819</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000819</idno><idno type="wicri:Area/PubMed/Curation">000783</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000783</idno><idno type="wicri:Area/PubMed/Checkpoint">000783</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000783</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Lack of miRNA Misregulation at Early Pathological Stages in Drosophila Neurodegenerative Disease Models.</title><author><name sortKey="Reinhardt, Anita" sort="Reinhardt, Anita" uniqKey="Reinhardt A" first="Anita" last="Reinhardt">Anita Reinhardt</name><affiliation wicri:level="3"><nlm:affiliation>Laboratoire de Génétique du Stress et du Vieillissement, Unité de Biologie Fonctionnelle et Adaptative, CNRS EAC 4413, Université Paris Diderot Sorbonne Paris Cité, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Laboratoire de Génétique du Stress et du Vieillissement, Unité de Biologie Fonctionnelle et Adaptative, CNRS EAC 4413, Université Paris Diderot Sorbonne Paris Cité, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Feuillette, Sebastien" sort="Feuillette, Sebastien" uniqKey="Feuillette S" first="Sébastien" last="Feuillette">Sébastien Feuillette</name></author><author><name sortKey="Cassar, Marlene" sort="Cassar, Marlene" uniqKey="Cassar M" first="Marlène" last="Cassar">Marlène Cassar</name></author><author><name sortKey="Callens, Celine" sort="Callens, Celine" uniqKey="Callens C" first="Céline" last="Callens">Céline Callens</name></author><author><name sortKey="Thomassin, Helene" sort="Thomassin, Helene" uniqKey="Thomassin H" first="Hélène" last="Thomassin">Hélène Thomassin</name></author><author><name sortKey="Birman, Serge" sort="Birman, Serge" uniqKey="Birman S" first="Serge" last="Birman">Serge Birman</name></author><author><name sortKey="Lecourtois, Magalie" sort="Lecourtois, Magalie" uniqKey="Lecourtois M" first="Magalie" last="Lecourtois">Magalie Lecourtois</name></author><author><name sortKey="Antoniewski, Christophe" sort="Antoniewski, Christophe" uniqKey="Antoniewski C" first="Christophe" last="Antoniewski">Christophe Antoniewski</name></author><author><name sortKey="Tricoire, Herve" sort="Tricoire, Herve" uniqKey="Tricoire H" first="Hervé" last="Tricoire">Hervé Tricoire</name></author></analytic><series><title level="j">Frontiers in genetics</title><idno type="eISSN">1664-8021</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Late onset neurodegenerative diseases represent a major public health concern as the population in many countries ages. Both frequent diseases such as Alzheimer disease (AD, 14% incidence for 80-84 year-old Europeans) or Parkinson disease (PD, 1.4% prevalence for >55 years old) share, with other low-incidence neurodegenerative pathologies such as spinocerebellar ataxias (SCAs, 0.01% prevalence) and frontotemporal lobar degeneration (FTLD, 0.02% prevalence), a lack of efficient treatment in spite of important research efforts. Besides significant progress, studies with animal models have revealed unexpected complexities in the degenerative process, emphasizing a need to better understand the underlying pathological mechanisms. Recently, microRNAs (miRNAs), a class of small regulatory non-coding RNAs, have been implicated in some neurodegenerative diseases. The current data supporting a role of miRNAs in PD, tauopathies, dominant ataxias, and FTLD will first be discussed to emphasize the different levels of the pathological processes which may be affected by miRNAs. To investigate a potential involvement of miRNA dysregulation in the early stages of these neurodegenerative diseases we have used Drosophila models for seven diseases (PD, 3 FTLD, 3 dominant ataxias) that recapitulate many features of the human diseases. We performed deep sequencing of head small RNAs after 3 days of pathological protein expression in the fly head neurons. We found no evidence for a statistically significant difference in miRNA expression in this early stage of the pathological process. In addition, we could not identify small non-coding CAG repeat RNAs (sCAG) in polyQ disease models. Thus our data suggest that transcriptional deregulation of miRNAs or sCAG is unlikely to play a significant role in the initial stages of neurodegenerative diseases.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">23115562</PMID><DateCreated><Year>2012</Year><Month>11</Month><Day>01</Day></DateCreated><DateCompleted><Year>2012</Year><Month>11</Month><Day>02</Day></DateCompleted><DateRevised><Year>2013</Year><Month>08</Month><Day>13</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1664-8021</ISSN><JournalIssue CitedMedium="Internet"><Volume>3</Volume><PubDate><Year>2012</Year></PubDate></JournalIssue><Title>Frontiers in genetics</Title><ISOAbbreviation>Front Genet</ISOAbbreviation></Journal><ArticleTitle>Lack of miRNA Misregulation at Early Pathological Stages in Drosophila Neurodegenerative Disease Models.</ArticleTitle><Pagination><MedlinePgn>226</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3389/fgene.2012.00226</ELocationID><Abstract><AbstractText>Late onset neurodegenerative diseases represent a major public health concern as the population in many countries ages. Both frequent diseases such as Alzheimer disease (AD, 14% incidence for 80-84 year-old Europeans) or Parkinson disease (PD, 1.4% prevalence for >55 years old) share, with other low-incidence neurodegenerative pathologies such as spinocerebellar ataxias (SCAs, 0.01% prevalence) and frontotemporal lobar degeneration (FTLD, 0.02% prevalence), a lack of efficient treatment in spite of important research efforts. Besides significant progress, studies with animal models have revealed unexpected complexities in the degenerative process, emphasizing a need to better understand the underlying pathological mechanisms. Recently, microRNAs (miRNAs), a class of small regulatory non-coding RNAs, have been implicated in some neurodegenerative diseases. The current data supporting a role of miRNAs in PD, tauopathies, dominant ataxias, and FTLD will first be discussed to emphasize the different levels of the pathological processes which may be affected by miRNAs. To investigate a potential involvement of miRNA dysregulation in the early stages of these neurodegenerative diseases we have used Drosophila models for seven diseases (PD, 3 FTLD, 3 dominant ataxias) that recapitulate many features of the human diseases. We performed deep sequencing of head small RNAs after 3 days of pathological protein expression in the fly head neurons. We found no evidence for a statistically significant difference in miRNA expression in this early stage of the pathological process. In addition, we could not identify small non-coding CAG repeat RNAs (sCAG) in polyQ disease models. Thus our data suggest that transcriptional deregulation of miRNAs or sCAG is unlikely to play a significant role in the initial stages of neurodegenerative diseases.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Reinhardt</LastName><ForeName>Anita</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Laboratoire de Génétique du Stress et du Vieillissement, Unité de Biologie Fonctionnelle et Adaptative, CNRS EAC 4413, Université Paris Diderot Sorbonne Paris Cité, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Feuillette</LastName><ForeName>Sébastien</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Cassar</LastName><ForeName>Marlène</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Callens</LastName><ForeName>Céline</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Thomassin</LastName><ForeName>Hélène</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Birman</LastName><ForeName>Serge</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Lecourtois</LastName><ForeName>Magalie</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Antoniewski</LastName><ForeName>Christophe</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Tricoire</LastName><ForeName>Hervé</ForeName><Initials>H</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>10</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front 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MajorTopicYN="N">neurodegenerative diseases</Keyword><Keyword MajorTopicYN="N">polyQ diseases</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year><Month>07</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2012</Year><Month>10</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>11</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>11</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>11</Month><Day>2</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23115562</ArticleId><ArticleId IdType="doi">10.3389/fgene.2012.00226</ArticleId><ArticleId IdType="pmc">PMC3483601</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Paris</li></settlement></list><tree><noCountry><name sortKey="Antoniewski, Christophe" sort="Antoniewski, Christophe" uniqKey="Antoniewski C" first="Christophe" last="Antoniewski">Christophe Antoniewski</name><name sortKey="Birman, Serge" sort="Birman, Serge" uniqKey="Birman S" first="Serge" last="Birman">Serge Birman</name><name sortKey="Callens, Celine" sort="Callens, Celine" uniqKey="Callens C" first="Céline" last="Callens">Céline Callens</name><name sortKey="Cassar, Marlene" sort="Cassar, Marlene" uniqKey="Cassar M" first="Marlène" last="Cassar">Marlène Cassar</name><name sortKey="Feuillette, Sebastien" sort="Feuillette, Sebastien" uniqKey="Feuillette S" first="Sébastien" last="Feuillette">Sébastien Feuillette</name><name sortKey="Lecourtois, Magalie" sort="Lecourtois, Magalie" uniqKey="Lecourtois M" first="Magalie" last="Lecourtois">Magalie Lecourtois</name><name sortKey="Thomassin, Helene" sort="Thomassin, Helene" uniqKey="Thomassin H" first="Hélène" last="Thomassin">Hélène Thomassin</name><name sortKey="Tricoire, Herve" sort="Tricoire, Herve" uniqKey="Tricoire H" first="Hervé" last="Tricoire">Hervé Tricoire</name></noCountry><country name="France"><region name="Île-de-France"><name sortKey="Reinhardt, Anita" sort="Reinhardt, Anita" uniqKey="Reinhardt A" first="Anita" last="Reinhardt">Anita Reinhardt</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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